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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Calcif Tissue Int. 1999 Mar;64(3):209-13.
Decreased estradiol levels and free androgen index and elevated sex hormone-binding globulin levels in male idiopathic osteoporosis.

Gillberg P, Johansson AG, Ljunghall S.

Department of Internal Medicine, University Hospital, S-751 85 Uppsala, Sweden.

Estrogen deficiency is an important pathogenetic factor in female osteoporosis, and androgens are known to have anabolic effects on bone. In this study we have compared 12 men with idiopathic osteoporosis, age 27-55 years, with 12 age-matched men, with respect to serum levels of sex steroids, biochemical markers of bone turnover, bone density, and body composition. All subjects showed values within the normal range for all hormonal parameters. The patient group compared with the controls had significantly lower serum levels of estradiol (71 +/- 13 versus 85 +/- 14 pmol/liter, P < 0.03); estradiol/sex hormone-binding globulin (SHBG) ratio (22.4 +/- 12.1 versus 39.5 +/- 18.6 pmol/mg, P < 0.02); free androgen index (51.0 +/- 19.4 versus 74.1 +/- 33.1%, P < 0.05); and higher SHBG (3.7 +/- 1.6 versus 2.5 +/- 1.0 mg/liter; P < 0.04). The men with idiopathic osteoporosis had significantly lower body mass index (23.2 +/- 2.8 versus 25.9 +/- 3.3 kg/m2, P < 0.05); and a tendency to lower percentage of total body fat (14.2 +/- 5.5 versus 18.6 +/- 6.0%; P < 0.10) than the controls. Regression analyses revealed that bone mineral density in femoral neck correlated significantly and positively with the ratio estradiol/SHBG (r = 0.67; P < 0.04) and negatively with SHBG concentrations (r = -0.63; P < 0.04) in the group of patients. These findings could represent a pathogenetic mechanism in male idiopathic osteoporosis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10024377&dopt=Abstract

Science. 1999 Feb 26;283(5406):1317-21.
Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators.

Yanagisawa J, Yanagi Y, Masuhiro Y, Suzawa M, Watanabe M, Kashiwagi K, Toriyabe T, Kawabata M, Miyazono K, Kato S.

Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.

Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10037600&dopt=Abstract

J Histochem Cytochem. 1999 Mar;47(3):289-302.
Cellular and subcellular expression of Golf/Gs and Gq/G11 alpha-subunits in rat pancreatic endocrine cells.

Astesano A, Regnauld K, Ferrand N, Gingras D, Bendayan M, Rosselin G, Emami S.

Unite de Recherches sur la Signalisation et les Fonctions Cellulaires: Paris, France.

We studied the cellular and subcellular localization of Galpha-subunits in pancreas by immunocytochemistry. Golfalpha and G11alpha were specifically localized in islet insulin B-cells and glucagon A-cells, respectively. Gsalpha and Gqalpha labeling was more abundant in B-cells. The presence of Golfalpha in B-cells was confirmed by in situ hybridization. In B-cells, Golfalpha and Gsalpha were found in the Golgi apparatus, plasma membrane (PM) and, remarkably, in mature and immature insulin secretory granules, mainly at the periphery of the insulin grains. Gqalpha was detected on the rough endoplasmic reticulum (RER) near the Golgi apparatus. In A-cells, the Galpha-subunits were mostly within the glucagon granules: G11alpha gave the strongest signal, Gsalpha less strong, Gq was scarce, and Golf was practically absent. Gqalpha and Gsalpha immunoreactivity was detected in acinar cells, although it was much weaker than that in islet cells. The cell-dependent distribution of the Galpha-subunits indicates that the stimulatory pathways for pancreatic function differ in acinar and in islet B- and A-cells. Furthermore, the G-protein subunits in islet cell secretory granules might be functional and participate in granule trafficking and hormone secretion.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10026232&dopt=Abstract

QJM. 1998 Nov;91(11):755-66.
Emergent immunoregulatory properties of combined glucocorticoid and anti-glucocorticoid steroids in a model of tuberculosis.

Hernandez-Pando R, de la Luz Streber M, Orozco H, Arriaga K, Pavon L, Marti O, Lightman SL, Rook GA.

Department of Pathology, Instituto Nacional de la Nutricion, Salvador Zubiran, Mexico City.

In Balb/c mice with pulmonary tuberculosis, there is a switch from a protective Th1-dominated cytokine profile to a non-protective profile with a Th2 component. This switch occurs while the adrenals are undergoing marked hyperplasia. Treatment with the anti-glucocorticoid hormones dehydroepiandrosterone or 3 beta, 17 beta-androstenediol, during the period of adrenal hyperplasia, maintains Th1 dominance and is protective. We investigated the effects of these hormones as therapeutic agents by administering them from day 60, when the switch to the non-protective cytokine profile was already well established. Given at this time (day 60), doses that were protective when given early (from day 0) were rapidly fatal. A physiological dose of the glucocorticoid corticosterone was also rapidly fatal. However when the corticosterone and the anti-glucocorticoid (AED or DHEA) were co-administered, there was protection, with restoration of a Th1-dominated cytokine profile, enhanced DTH responses, and enhanced expression of IL-1 alpha and TNF alpha. Therefore this combination of steroids has an emergent property that is quite unlike that of either type of steroid given alone. It may be possible to exploit the ant-inflammatory properties of glucocorticoids while preserving a Th1 bias, by combining glucocorticoids with DHEA or suitable metabolites.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10024939&dopt=Abstract

J Nephrol. 1998 Nov-Dec;11(6):289-95.
Dietary salt intake, blood pressure and the kidney in hypertensive patients with non-insulin dependent diabetes mellitus.

Campese VM, Wurgaft A, Safa M, Bianchi S.

Department of Medicine, University of Southern California, Los Angeles, USA. campessc.usc.edu

The mechanisms responsible for hypertension in NIDDM patients are only partially understood. Increased sensitivity to dietary salt intake and to vasoconstrictor hormones are among the mechanisms proposed. We have studied 19 hypertensive NIDDM patients 7 salt-sensitive and 12 salt-resistant while they were ingesting a diet with 20 mEq/day of Na+ for 9 days and while they were ingesting a diet containing 250 mEq/day of Na+ for 14 days. During the last 4 days of each dietary regimen, they received 60 mg/day of slow-release nifedipine. Blood pressure response to increasing doses of norepinephrine and angiotensin II was studied at the end of each of the four phases of the study. High salt intake increased blood pressure and decreased heart rate in these patients. High salt intake also increased the vascular response to norepinephrine but not to angiotensin II in NIDDM hypertensive subjects. Glomerular filtration rate and renal blood flow were not different during the low and high salt diets. There were no differences in the blood pressure response to norepinephrine or angiotensin II, nor in renal hemodynamic changes among salt-sensitive and salt-resistant NIDDM patients. Nifedipine decreased blood pressure equally in salt-sensitive and salt-resistant hypertensive patients and during the high and the low salt intake. Nifedipine increased renal blood flow, both in salt-sensitive and in salt-resistant individuals, but the differences did not reach statistical significance. Nifedipine decreased the blood pressure response to both norepinephrine and angiotensin II. The studies indicate that an increased reactivity to the pressor action of norepinephrine may contribute to the maintenance of hypertension in NIDDM hypertensive subjects and high salt intake may aggravate the pressor responsiveness to norepinephrine in these patients. Nifedipine is an effective antihypertensive drug in NIDDM patients and its action may be in part related to a decrease in pressor response to norepinephrine and angiotensin II.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10048494&dopt=Abstract

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DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.

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